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Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
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Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
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Delayed Graft Function and the Renin-angiotensin System.

Fatmah Yamani1, Cosimo Cianfarini, Daniel Batlle

  • 1Division of Nephrology, Northwestern University Feinberg School of Medicine, Chicago, IL.

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|February 16, 2024
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Summary

Delayed graft function (DGF) after kidney transplant involves renin-angiotensin system (RAS) activation. Targeting RAS, particularly with angiotensin-converting enzyme 2, may prevent DGF and improve transplant outcomes.

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Area of Science:

  • Nephrology
  • Transplantation immunology
  • Renal physiology

Background:

  • Delayed graft function (DGF) is a common complication of kidney transplantation, leading to poor patient outcomes and increased costs.
  • Currently, no specific treatments exist for DGF, a form of acute kidney injury (AKI).
  • Activation of the renin-angiotensin system (RAS) is implicated in the development of DGF.

Purpose of the Study:

  • To review the role of RAS activation in the pathophysiology of DGF.
  • To examine RAS involvement across all stages of kidney transplantation, including procurement, preservation, implantation, and reperfusion.
  • To explore potential therapeutic strategies targeting the RAS for DGF prevention.

Main Methods:

  • Review of existing literature on DGF and RAS activation.
  • Analysis of data from experimental animal models of kidney transplantation and AKI.
  • Discussion of the role of angiotensin-converting enzyme 2 (ACE2) in RAS regulation and kidney injury.

Main Results:

  • RAS activation can occur in deceased donors and is potentiated during organ procurement and preservation.
  • RAS is activated during kidney graft implantation and reperfusion in recipients.
  • ACE2 plays a crucial role in metabolizing angiotensin II and is present at the primary injury site in DGF.

Conclusions:

  • RAS activation significantly contributes to DGF pathophysiology.
  • Targeting RAS, potentially through ACE2-based interventions, offers a promising therapeutic avenue for preventing DGF.
  • Further research into RAS modulation could lead to improved kidney transplant outcomes.